The amygdala is a subcortical temporal lobe structure that plays a critical role in the modulation of social behavior and the recognition and production of emotion. Because these functions are among the most impaired in autism, the amygdala has long been considered a potential locus of pathology. Abnormal postnatal enlargement has been observed in the autistic amygdala via structural magnetic resonance imaging, but no consistent difference in macrostructural volume has been observed in adults. The cellular abnormalities underlying these volumetric changes have remained largely undescribed, but a decreased number of neurons has been reported in adults with autism. What cellular alterations might be present such that a reduction in neuron number does not result in a detectable decrease in amygdala volume? One strong possibility is microglial activation, which would cause increases in glial density and somal volume;these alterations may be present in other regions of peak developmental macrostructural and functional abnormality in autism. We will conduct a stereological count of microglial number, apply isotropic nucleator to calculate average microglial somal cross-sectional area, and carry out a spatial pattern analysis of the degree of microglia-neuron clustering as well as neuron-neuron clustering. These assessments will be conducted in cases in which neuron loss has already been observed, allowing us to relate glial and neuronal alterations. Another possible explanation is an increase in the space occupied by dendritic arbors and axons i.e. neuropil. However, the normal developmental course of dendritic arborization in the amygdala has not been established. Thus, we will examine the postnatal development of the dendritic arbors of amygdala neurons in a rhesus monkey model, and relate this development to the degree of neuron-neuron clustering. Previous assessments performed in the same primates include stereological analysis of neuron number and volume in the contralateral amygdala and macrostructural volume assessment via structural MRI. In our human subjects, a finding of microglial activation in the same brains as neuron loss might lead to direct therapeutic benefit for individuals in whom this activation is taking place. Our description of cellular abnormalities will further advance the field's understanding of the neuropathology underlying this disorder, pointing the way toward improved animal models and the development of better biomarkers. Our primate study will serve as a reference point for all future human studies of abnormal neuronal and neuropil development in the amygdala in multiple neuropsychiatric disorders.